Dr. TP Chhangte discusses anterior uveitis, including its definition, epidemiology, classification, pathology, clinical features, complications, and differential diagnosis. Some key points: - Anterior uveitis is inflammation of the iris and anterior part of the ciliary body. Its prevalence has been increasing and it commonly affects people aged 20-50. - Uveitis can be classified anatomically, clinically, etiologically, and pathologically. The anatomical classification divides uveitis into anterior, intermediate, posterior, and panuveitis based on location of inflammation. - Clinical features of anterior uveitis include eye pain, redness, photophobia, and decreased vision. On examination

1. Dr TP Chhangte
ANTERIOR UVEITIS

2. DEFINITION
 Inflammation of iris and anterior part of
ciliary body (pars plicata), as a
consequence of diverse stimuli.

3. EPIDEMIOLOGY
 The prevalence of uveitis which was estimated to be
around 17.4 per 100,000 population in 1960’s, in a
more recent investigation has been reported to be
52.4 per 100,000 people and the incidence seems
upraising
 It usually affects people 20-50 years of age and
account for 10-15% of cases of legal blindness in
developed countries. It is often combined with
autoimmune diseases and characterised by its
severe complications and recurrencythe
 most common presentation for uveitis is undoubtedly
acute anterior uveitis or AAU .AMERICAL UVEITIS
SOCIETY
 HLAB27 antigen is the commonest factor responsible
for uveitis in caucasians; in the afro-caribbean
community, sarcoidosis is common while Behcet’s
disease affects those of asian and middle eastern

4. CLASSIFICATION
 WHY TO CLASSIFY?
 Uvea consist of three continuous but distinct parts
 Uveitis may be caused by vast number of highly
variable conditions
 Uveitis may be one of the features of a serious or
life threatening systemic disease
 Uveitis is an entity for which no causative agent
may be found, despite most thorough diagnostic
investigations, in a number of cases
 Proper classification is essential if one is to avoid
confusion & misinterpretation

5.  ANATOMIC CLASSIFICATION
 CLINICAL CLASSIFICATION
 PATHOLOGIC CLASSIFICATION
 ETIOLOGIC CLASSIFICATION

6. ANATOMIC CLASSIFICATION
 Anterior uveitis
Inflammation of iris & ciliary body, inflammatory
cells in anterior chamber, minimal spillover into
retrolental space
 Intermediate uveitis
Ocular inflammation primarily involves
parsplana & peripheral retina, inflammatory cells
in anterior vitreous
 Posterior uveitis
Inflammation of retina or choroid primarily
 Panuveitis
Inflammation involving all anatomic segments of
the uvea

7. International uveitis study group
Anterior uvetis Intermediate
Uveitis
Posterior
uveitis
Panuveitis
Iritis Posterior cyclitis Focal, multifocal
or diffuse
choroiditis
Anterior cyclitis Hyalitis Choroiretinitis or
retinochoroiditis
Iridocyclitis Basal
retinochoroiditis
Neuroretinitis

8. SUN working group
Anterior uveitis Intermediate
uveitis
Posterior
uveitis
Panuveitis
Iritis Posterior cyclitis Focal, multifocal
or diffuse
choroiditis
Anterior cyclitis Hyalitis Retinitis,
Choroiretinitis or
retinochoroiditis
Iridocyclitis Pars planitis Neuroretinitis

9. Immunology & uveitis service,
Massachusetts eye & ear infirmary
Harvard Medical school
Anterio
r uveitis
Intermediat
e
uveitis
Posterior
uveitis
Panuveit
is
Sclerouveiti
s
Keratouveiti
s
Iritis Iridocyclitis Focal,
multifocal,
or diffuse
choroiditis
Uveitis &
scleritis
Uveitis &
keratitis
Cyclitis chorioretiniti
s
Fuch’s
heterochromi
c
iridocyclitis
Retinochoro
iditis
Phacogenic
uveitis
Retinal
vasculitis
Pars planitis Neuroretiniti
s

10. Kessler classification
Sclerouveiti
s
Keratouveiti
s
Anterior
uveitis
Intermediate
uveitis
Posterior
uveitis
Iritis Cyclitis Retinitis
Iridocyclitis Vitritis Choroiditis
Pars planitis

11. CLINICAL CLASSIFICATION
 Acute uveitis – sudden symptomatic onset.
Persists for 6 weeks or less
 Recurrent: Repeated episodes separated by
periods of inactivity without treatment > 3 months’
duration
 Chronic uveitis: Insidious onset & longer
than 6 weeks
(limited udration < 3 months & persistent disease
> 3 months)

12. PATHOLOGIC CLASSIFICATION
Pathologic
classification
Non
suppurative
Granulomatous
Non
granulomatous
Suppurative

13. Granulomatous inflammation
 Granulomatous inflammation
is a distinctive type of chronic
inflammatory reaction in which
the predominant cell type is an
activated macrophage with a
modified epithelial-like
appearance
 Granuloma is a focal area of
granulomatous inflammation
consisting of an aggregation of
macrophages, which may or may
not be surrounded by mononu
clear leukocytes

14. Pathological classification
Granulomatous Non-granulomatous
1. Aetiology Organismal invasion Antigen – antibody
rection
2. Course
a) Onset Insidious Acute
b) Duration Chronic Short
c) Inflammation Moderate Severe
3. Pathology
a) Lesion Circumscribed Diffuse
b) Iris Focal reaction Diffuse reaction
c) Keratic precipitates Mutton fat Fine plenty
d) Iris adhesions Coarse, few, thick Fine, plenty, thin
4. Investigations May be positive negative

15.  Mutton fat Keratic precipitates (KPs)
 Koeppe iris nodules
 Busacca iris nodules

16. ETIOLOGICAL
CLASSIFICATION
 IUGS CLINICAL CLASSIFICATION OF UVEITIS
 INFECTIOUS
Bacterial
Viral
Fungal
Parasitic
Others
 NON-INFECTIOUS
Known systemic association
No known systemic association
 MASQUERADE
Neoplastic
Non-neoplastic
 TRAUMATIC

17. ETIOLOGICAL
CLASSIFICATION
DUKE ELDER’S CLASSIFICATION
1. Infective uveitis
2. Immune-related uveitis
3. Toxic uveitis
4. Traumatic uveitis
5. Uveitis associated with non-infective systemic
diseases
6. Idiopathic uveitis

18. ETIOLOGICAL
CLASSIFICATION
 1)Exogenous –
Introduction of organism into the eye through a
perforating wound or ulcer  acute iridocyclitis of
suppurative type, pan ophthalmitis
 2) Secondary infection –
Due to direct spread from adjoining structures –
CORNEA
SCLERA
RETINA

19.  3)Endogenous
Bacterial e.g. TB, syphilis, gonorrhea
Viral e.g., Mumps, small pox, influenza
Protozoal e.g., toxoplasmosis
 4) Antigen-antibody reaction
Result of an antigen-antibody reaction occuring in
the eye due to previous sensitization of uveal
tissue to some allergen. The allergen is a foreign
protein
 Most of the cases of iridocyclitis do not have
any specific cause and are probably allergic in
nature

20.  5)Auto-immune -
a)Immune disorders affecting the body as a
whole have ocular manifestations in the
form of iridocyclitis.
e.g. rheumatoid arthritis, SLE, ankylosing
spondylitis, Reiter’s syndrome, Behcet’s
Syndrome.
b) response to antigenic stimuli in other part of
the eye. Iridocyclitis is a common
accompaniment of severe corneal infection
and choroiditis of retinal inflammation.
 HLA antigenic involvement
 Disproportionately high percentage of
patients of B-27 antigenic group develop

21. SPECIFIC CLINICO-ETIOLOGICAL TYPES
OF NON-SUPPURATIVE UVEITIS
 I. UVEITIS ASSOCIATED WITH CHRONIC
SYSTEMIC BACTERIAL INFECTIONS:
1. Tubercular uveitis
2. Syphilitic uveitis
3. Leprotic uveitis
 II. UVEITIS ASSOCIATED WITH NONINFECTIOUS
SYSTEMIC DISEASES
1. Uveitis in sarcoidosis
2. Behcet’s disease.
 III. UVEITIS ASSOCIATED WITH ARTHRITIS
1. Uveitis with Ankylosing spondylitis
2. Reiter’s syndrome
3. Still’s disease
 IV. PARASITIC UVEITIS
1. Toxoplasmosis
2. Toxocariasis
3. Onchocerciasis
4. Amoebiasis
 V. FUNGAL UVEITIS
1. Presumed ocular histoplasmosis
syndrome
2. Candidiasis
 VI. VIRAL UVEITIS
1. Herpes simplex uveitis
2. Herpes zoster uveitis
3. Acquired cytomegalovirus uveitis
4. Uveitis in acquired immune deficiency
syndrome (AIDS)
 VII. LENS INDUCED UVEITIS
1. Phacotoxic uveitis
2. Phacoanaphylactic endophthalmitis
 VIII. TRAUMATIC UVEITIS
 IX. UVEITIS ASSOCIATED WITH MALIGNANT
INTRAOCULAR TUMOURS
 X. IDIOPATHIC SPECIFIC UVEITIS
SYNDROMES
1. Fuchs’ uveitis syndrome
2. Intermediate uveitis (pars planitis)
3. Sympathetic ophthalmitis (see page 413-
414)
4. Glaucomatocyclitic crisis.
5. Vogt-Koyanagi-Harada’s syndrome.
6. Bird shot retinochoroidopathy.
7. Acute multifocal placoid pigment epitheliopathy
(AMPPE)
8. Serpiginous choroidopathy.

22. PATHOLOGY AND CLINICAL
SIGNS-
Inflammation of iris and ciliary body
Dilatation of blood vessels
Iris stromal edema.
SIGNS - Iris pattern altered.Iris colour altered. Iris
thickened.Also accompanied by, ciliary
congestion, conjunctival hyperaemia and
chemosis of conjunctiva.

23. Exudation of fibrin-rich fluid and inflammatory
cells in the tissues
Exudates escape into anterior chamber
 Plasmoid aqueous
 SIGNS - Aqueous flare (like the beam of projector in
smokey theatre) and Cells

24. Nutrition of corneal endothelium is affected due
to toxins
Corneal endothelium becomes sticky and
edematous
Cells desquamated at places
Inflammatory cells stick to endothelial layer as
cellular deposits
SIGN – Keratic precipitates

25.  In very intense cases, polymorphs pour out to
sink to bottom of anterior chamber
 SIGN – Hypopyon

26. Exudates cover the iris as a thin film and spread over
pupillary area
SIGN – Irritation of iris musculature constrictor
being more powerful than dilator, spasm results in
miosis.
If exudate is profuse
SIGN – Plastic iritis
Blockage of pupil
SIGN – impairment of sight

27. In early stages, there is adhesion of iris to lens capsule
(Atropine may free the iris)
SIGN – Spots of exudate or pigment derived from
posterior layer of iris left permanently upon
anterior capsule of lens (valuable evidence of
previous iritis)
Later on, the organization of the adhesion leads to
formation of fibrous bands between pupillary margin
of iris and lens capsule (atropine cannot rupture them)
SIGN – Posterior synechiae (more in lower part of
pupil due to effect of gravity)

28.  When adhesions are localized and a
mydriatic is instilled, it causes
intervening portions of circle of pupil to
dilate.

29. Pigment epithelium on posterior surface is
pulled around pupillary margin so that
patches of pigment on anterior surface
of iris are seen.
SIGN – Ectropion of uveal pigment
(due to contraction of organizing
exudates upon iris)
With recurrent attacks or severe cases,
the whole circle of pupillary margin gets
tied to lens capsule.
SIGNS – Annular or ring synechiae
or Seclusio pupillae

30. Collection of aqueous behind iris since aqueous
drainage is hampered.
Iris is hence bowed forwards like sail.
 SIGN – Iris Bombe (anterior chamber is
funnel shaped i.e. deepest in centre,
shallowest at periphery)

31. As iris bulges forward and comes into contact
with cornea
Adhesions of iris to cornea at periphery
develop
SIGNS – Peripheral anterior synechiae
Obliteration of filtration angle (Hypertensive
iridocyclitis)
SIGNS – Rise in IOT (secondary glaucoma)

32. When exudate is more extensive
Organization of exudate across entire pupillary
area
Film of opaque fibrous tissue in pupillary area
SIGNS – Occlusio pupillae or Blocked pupil
Exudates fill up posterior chamber if there is
much of cyclitis
When these adhesions organize, the iris
adheres to lens capsule.
SIGNS – Total posterior synechiae

33. When these adhesions organize, the iris
adheres to lens capsule.
SIGNS – Total posterior synechiae
Retraction of peripheral part of iris
Anterior chamber is abnormally deep at
periphery
In worst cases of plastic iridocyclitis

34. Cyclitic membrane formed
behind lens
Finally, degenerative
changes in ciliary body
Vitreous becomes fluid
Nutrition of lens impaired
SIGNS – Complicated
cataract

35. In final stages, there is
interference with
secretion of aqueous
Fall in IOT
Eye shrinks
(development of soft
eye is an ominous
sign)
SIGNS – Phthisis bulbi

36. MEDICAL HISTORY
TABLE: Medical history factors in Diagnosis of Uveitis
Modifying factors Associated factors suggesting
systemic conditions
Time course of disease
Acute
Recurrent
Chronic
Immune system status
Systemic medications
Trauma history
Travel hisotry
Severity
Severe
Inactive
Social history
Eating habits
Pets
Distribution of uveitis
Unilateral
Bilateral
Alternating
Focal
Multifocal
Diffuse
Sexual practices
Occupation
Drug use
Patient’s sex
Patient’s age
Patient’s race

37. SYSTEMIC EVALUATION
 Skin
 Joints
 Lung
 Neurologic
 GI
 GU

38. CLINICAL FEATURES
SYMPTOMS
 Pain
 Diminished vision
 Redness of eye
 lacrimation
 photophobia
 haloes around light
SIGNS
 Injection
 Keratic precipitate
(KP)
 Iris nodule
Koeppe, Busacca
 Cells (AC or vitreous)
 Flares
 Posterior synechiae
(PS)

39. SEVERITY OF ANTERIOR
UVEITIS

40. SIGNS OF ACUTE ANTERIOR UVEITIS

42.  Iris nodules in granulomatous
anterior uveitis
(A) Koeppe nodules
(B) Busacca nodules

43. CELLS & FLARE
Cells: active inflammation
Flare: leakage of protein

44. DIFFERENTIAL DIAGNOSIS
Character Conjunctivitis Iridocyclitis ACG
Infection Superficial Deep ----
Secretion Mucopurulent Watery Watery
Pupil Normal Small, irregular Large, oval
Media Clear Sometimes pupil
opaque
Corneal oedema
Tension Normal Usually normal High
Pain Mild Moderate
with first division
of trigeminal
Severe and
entire trigeminal
Tenderness Absent Marked Marked
Vision Good Fair Poor
Onset Gradual Usually gradual Sudden
Systemic
complications
Absent Little Prostration
& vomiting

45. COMPLICATIONS OF UVEITIS
 Hypertensive uveitis – Secondary glaucoma
 Endothelial opacities in cornea due to
formation of keratic precipitates
 Hypopyon and hyphaema
 suppurative uveitis may progress to end-
ophthalmitis or pan-ophthalmitis
 toxic matter goes into lens – complicated
cataract.
 Post inflammatory atrophy of zonules –
subluxation of lens
 vitreous – opacification of vitreous,
liquification of gel, shrinkage of gel, retinal
detachment

46.  macular edema
 optic neuritis – undergoes atrophy – optic
nerve atrophy
 occlusive pupillae
 seclusion pupillae
 ectropion of uveal pigment
 hypotony – atrophic bulbi
 secondary squint
 iris atrophy

47. Uveitis and Systemic Disease – avoid a shotgun
approach to investigation!!
Do not wade in like John Wayne!!

48. When to investigate?
 One of the most pressing questions that arises in
the mind of every ophthalmologist who sees a
new case of uveitis is “what is the cause of this
disease?” In evaluating patients with uveitis, the
ophthalmologist must consider that a lengthy list
of infections, autoimmune systemic diseases,
distinctive inflammatory conditions and
masquerade syndromes may all cause uveal
inflammation. Despite this array of potential
diagnoses, the vast majority of patients have
disease that defies categorisation

49. SPECIAL INVESTIGATIONS
 INDICATIONS
Granulomatous inflammation.
Recurrent uveitis.
Bilateral disease.
Systemic manifestations without a specific
diagnosis.
Confirmation of a suspected ocular picture
which depends on the test result as part of
the criteria for diagnosis such as HLA-A29
testing for birdshot chorioretinopathy

50. INVESTIGATIONS
 Local
 vision, refraction, fundus examination
 IOT by Schiotz Tonometer
 Slit Lamp examination
 Focal –
 ENT, Dental, Genito-urinatory examination for
septic focus.

51. SKIN TEST
(A) Positive tuberculin skin reaction
(B) Strongly positive tuberculin skin react
(C) Positive pathergy test in Behcet synd

52.  For associated systemic disorders –
 CBC, ESR, MT, X-ray chest – Tuberculosis
 Urine, Blood examination-Diabetes
 VDRL, Kahn Test – syphilis
 Urethral smear – gonorrhoeae
 Urine culture – for UTI
 Blood culture – Septicemia
 ASLO Titre, C-reactive protein – for rheumatic
disorders
 Screening test for auto immune disorders
 Imaging :- FFA, ICGA, OCT, Sacroiliac joint x
ray, CT and MRI

54. Diagnosis of uveitis
 Find curable uveitis:
Trauma; infection; Neoplasm
 Find controllable disease
Systemic associated ocular inflammation
rheumatoid arthritis; lupus
Specific ocular inflammation

55. Diagnosis of uveitis
Find curable uveitis
Trauma : Hx
Infection:
Bacteria (complete blood count; culture)
Fungus (complete blood count; culture, culture)
Parasite (complete blood count; culture, eosinophil)
Virus: PCR; Serology: VDRL, HIV, Torch marker
 Neoplasm:
CBC, image study( PET)

56. Diagnosis of uveitis
Find controllable disease
• Systemic associated ocular inflammation:
 ankylosing spondylitis( image study, HLA-B27)
 Rheumatoid arthritis ( image study; CRP,RF)
 lupus( CBC; anti-ds DNA)
 sarcoidosis( CxR; biopsy)
 Behcet disease (oral ulcer,genital ulcers)
• Specific ocular inflammation
 Vogt-Koyanagi-Harada's Disease
 Sympathetic ophthalmia

57. CAUSES OF ANTERIOR
UVEITIS
ACUTE ANTERIOR UVEITIS(AAU) CHRONIC ANTERIOR
UVEITIS(CAU)
Idiopathic Juvenile rheumatoid arthritis
Trauma Fuchs’ Heterochromic Iridocyclitis
HLAB27 associated uveitis
Ankylosing spondylitis
Inflammatory bowel disease
(crohn’s ds &
ulcerative colitis)
Psoriatic arthritis
Reiter’s syndrome
Anterior uveitis associated with
Primary Posterior uveitis
Sarcoidosis
Toxoplasmosis
syphilis
tuberculosis
herpes zoster
CMV
AIDS
Behcet’s disease/syndrome OTHER POSTERIOR PROBLEMS
like RD
Lens-associated anterior uveitis
Phacoanaphylactic & phacogenic
Phacolytic
UGH syndrome

58. TRAUMATIC ANTERIOR
UVEITIS
 Trauma is one of the most common causes of
anterior uveitis
 There is usually a h/o blunt trauma to the eye or
adnexa
 Other injuries such as ocular burns, foreign
bodies or corneal abrasions may also result in
uveitis
 VA and IOP may be affected
 There may be hyphaema

59. IDIOPATHIC ANTERIOR
UVEITIS
 The term ‘Idiopathic’ applies to anterior uveitis
with no obvious systemic or tramatic etiology
 Diagnosis is established after exclusion of other
causes by history and examination

60. Ankylosing Spondylitis
 Characterized by inflammation, calcification and
finally ossification of ligaments and capsules of
joints with resultant bony ankylosis of the axial
skeleton
 Typically affects males, of whom 90% are HLA-
B27 positive
 3-4th decade, with insidious onset of pain and
stiffness in the lower back or buttock
 SIGNS: a) Spondyloarhritis b) enthesopathy
 RADIOLOGY: bamboo spine
 AAU occurs in 25% of pts with AS; conversely
25% of males with AAU will have AS

62. Reiter Syndrome
 Young adult male (3rd decade of life)
 Episode of arthritis of more than 1 month duration
 About 85% are + for HLA-B27
 Classic triad
Non-gonococcal Urethritis
Seronegative Polyarthritis(mostly knee, ankles
and toes)
Conjunctivitis (the most common) or acute iritis
(12%)
 Ocular features
- Bilateral mucopurulent conjunctivitis
- Acute anterior iritis
- Punctate epithelial keratitis
Keratoderma blenorhagica
Circinate balanitis

63. Psoriatic arthritis
 About 7% of pts with psoriasis develop arthritis;
3-4th decade
 HLA-B27, HLA-B17
 SIGNS: SKIN (plaque & flexural); NAIL
(pitting+transverse depression and onycholysis);
ARTHRITIS (asymmetrical and distal IPJ)
 Ocular features:
- Conjunctivitis
- Acute iritis(seen in 7%)
- Keratitis
- Secondary
sjorgen’s syndrome

64. Behcet Syndrome (1)
 Idiopathic, multisystem disease characterized by
recurrent episodes of orogenital ulceration
Generalized occlusive vasculitis
 Posterior involvement > Anterior
retinal vasculitis, hemorrhage, necrosis,
macular edema, ischemic optic neuropathy

65. (A) Major aphthous ulceration;
(B) genital ulceration;
(C) superficial thrombophlebitis
(D) dermatographia

67. Behcet Syndrome (2)
 Skin lesion: erythema nodosum
 HLA-B51
 Young adults
 Recurrence
 Poor prognosis
 T/t:
1. Steroid 2. Immunosuppressor

68. Glaucomatocyclitic Crisis
(Posner- Schlossman Syndrome)
 a disease typified by acute, unilateral, recurrent attacks of
elevated intraocular pressure (IOP) accompanied by mild
anterior chamber inflammation.
 S/S: KP, IOP elevation
 Eti: still unknown; autoimmune to infectious
; prostaglandin induced trabeculitis
 Dx: clinical criteria
1. Fine KP 2. trabeculitis
3. IOP elevation
TX: 1. Steroid
2 atropine
3 control IOP
4 avoid miotic
5 avoid prostagradin

69. Lens-Associated Uveitis
 Phacoantigenic glaucoma and phacoanaphylactic
glaucoma
Lens capsule injury (immune response to
lens protein)
Mutton-fat KP, dense cells & flare, PS
 Phacolytic glaucoma
Intact capsule, hypermature cataract
Acute increase of IOP (clogging of TM by
lens protein & engorged macrophages)
Lack of KP, PS
 UGH syndrome

70. Juvenile Idiopathic arthritis
 Idiopathic, inflammatory arthritis of at least 6 wks duration
before 16 yrs of age
 M:F 2:3
 Seronegative for IgM rheumatoid factor
 Presentation:
- Systemic onset(20%): transient maculopapular
rash, genelarized lymphadenopathy, hepato
splenomegaly and serositis
- Pauciarticular onset (60%)
- Polyarticular onset (20%)
 Ocular findings:- asymptomatic, uninjected white eye even
in the presence of severe uveitis, KPs are usually small to
medium- Posterior synechiae
 Complications: cataract (84%), band keratopathy (70%),
macular edema, vitreous debris, glaucoma, phthisis
 Treatment: topical steroids

71. Fuchs heterochromic iridocyclitis
 Chronic u/l uveitis
 TRIAD:
- heterochromia
- predisposition to cataract and glaucoma
- KPs
 Symptoms vary from none to mild blurring or
discomfort
 ETIOLOGY: NO SINGLE THEORY; Toxoplasma
gondii, HSV, Rubella, neurogenic causes and
autoimmune
 Complications: glaucoma, cataract, decreased
VA, iris atrophy

72. TREATMENT
1. of iridocyclitis
2. of complications and sequelae

73. Treatment of Iridocyclitis
Drugs used –
 Mydriatics
 Steroids ( topical, periocular injection,
systemic )
 Calcineurin inhibitors (Cyclosporin, Tacrolimus )
 Antimetabolites: (Azathioprine, MTX)

74. MYDRIATICS
 PREPARATIONS
 1. Short-acting
 Tropicamide (0.5 and 1%) has a duration of 6
hours
 Cyclopentolate (0.5% and 1%) has a duration of
24 hours
 Phenylephrine (2.5% and 10%) has a duration of
3 hours but no cycloplegic effects
 2. Long-acting:
 Homatripine 2% has a duration of 2 days
 Atropine 1% is the most powerful cycloplegic and
mydriactic with a duration of action lasting upto 2
weeks. Use of atropine may lead to PAC (SEC

75. Mydriatics
 Acts in 3 ways
 by keeping the iris and ciliary body at rest
 by diminishing hyperaemia
 by preventing formation of posterior synechiae
and breaking down any already formed

76. Essentials of treatment of anterior
uveitis
 Dilatation of pupil with atropine
 Hot application
 Control of acute phase of inflammation with
steroids

77. Method of administration and
dose
 Atropine may be used in form of drops or ointment
(1%) ,every four hours is usually sufficient.
 When pupil is well dilated, twice a day suffices.
 If atropine irritation ensues, one or the other
substitutes for this drug may be used.
e.g. Homatropine, Cyclopentolate.
 Mydriasis -the sub-conjunctival injection of 0.3 ml. of
mydricaine, a mixture of atropine, procaine and
adrenaline.
 To avoid relapse-Atropine, or its equivalent -continued
for at least 10 days to a fortnight after the eye
appears to be quiet

78.  Hot application
 extremely soothing to patient by diminishing the
pain.
 of therapeutic service in increasing the
circulation.

79. Corticosteroids
 Mainstay of treatment
 Dexamethasone, Bethamethasone, prednisolone
 Administered as drops or ointment, or more
effectively as subconjunctival injections are of great
value in controlling the inflammation in the acute
phase.
 Occasionally, results are dramatic and eye
becomes white with great rapidity.
 Minimize damages of antigen antibody reaction.

80. Corticosteroids
 INDICATIONS OF SYSTEMIC ADMINISTRATION
 Severe acute anterior uveitis, especially in
patients with ankylosing spondylitis with a marked
fibrinous exudate in the anterior chamber or
hypopyon
 As an adjunct to topical or systemic therapy in
resistant chronic anterior uveitis
 Poor patient compliance with topical or systemic
medication
 At time of surgery in eyes with uveitis

81. Aspirin
 Is very useful in relieving pain but if it is intense,
stronger preparation are required

82. IMMUNOSUPPRESSIVE
AGENTS
 Immunosuppressive agents used in the
treatment of uveitis are (a) antimetabolites
(Cytotoxics) and (b)
T-cell inhibitors
 Indications
1. Sight threatening uveitis : which is
usually b/l, non infectious, reversible and
has failed to respond to adequate steroid
therapy
2. Steroid sparing therapy:in patients with
intolerable side effects from systemic

83. Treatment of refractory uveitis
Conventional therapies

84. Treatment of complications and
sequelae-
 Secondary glaucoma-
 Before formation of posterior or peripheral
synechiae,- intensify atropinisation in order to
allay the inflammatory congestion.
 Corticosteroids - topically and acetazolamide -
systematically are very useful in such cases..

85. Annular synechiae-
 Iridectomy ‘
 ( No operative procedure of this kind must
be undertaken during an acute attack of
iritis if it can be avoided. Reason –
operation will set up a traumatic iritis which
will result in the opening getting filled with
exudates.)
 preventive iridectomy- Since ring
synechiae is the result of recurrent attacks,
iridectomy can be performed during
quiescent interval.
 Difficulty – iris is atrophied, friable.
Haemorrhage is common. Synechiae can

86.  Hypopyon and Hyphaema may need
evacuation and A.C. Wash.
 End-ophthalmitis – intravitreal injection of
Decadron and Gentamicin
 Pan ophthalmitis – Evisceration
 Iris Bombe
Medical – 1. Atropine 2. Diamox
Surgical – 1. 4-dot Iridotomy
 using von Graefe’s knife
 YAG Laser for breaking posterior synechiae